Recent Advances in the Effects of Chemical and Non-Chemical Exposures on the Kidney

A special issue of Toxics (ISSN 2305-6304). This special issue belongs to the section "Exposome Analysis and Risk Assessment".

Deadline for manuscript submissions: 25 October 2024 | Viewed by 937

Special Issue Editors


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Guest Editor
School of Public Health, Department of Environmental and Occupational Health, University of Pittsburgh, Pittsburgh, PA, USA
Interests: global environmental health research; research training; climate; health impact on vulnerable populations
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Guest Editor
Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA
Interests: environmental toxicants; chronic kidney disease

Special Issue Information

Dear Colleagues,

Environmental chemicals and non-chemical stressors, including heat stress, cause deteriorating kidney health. This Special Issue aims to enhance our understanding of the cumulative risk factors that influence kidney function and diseases throughout a person’s life.

A growing list of environmental chemicals pose significant challenges to kidney health, including toxic and essential trace elements, per- and polyfluorinated alkyl substances (PFAS), pesticides, persistent organic pollutants (POPs), nano-plastics, and other nano- or micro-particles. Additional converging factors play pivotal roles in promoting kidney disease and dysfunction, such as heat stress, humidity, adverse birth outcomes (such as a low birth weight and preterm birth), pregnancy-related conditions, like hypertensive disorders and diabetes, as well as social determinants of health.

The Special Issue will encompass a wide range of research articles, including basic science, translational, and epidemiological studies. With this collection of studies, we aim to shed light on recent advancements in the field of environmental kidney health.

Dr. Firoz Abdoel Wahid
Dr. John Danziger
Guest Editors

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Keywords

  • environment
  • kidney
  • nephron
  • pesticide
  • metal
  • heat
  • climate

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Published Papers (1 paper)

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Research

15 pages, 1609 KiB  
Article
Increased Prorenin Expression in the Kidneys May Be Involved in the Abnormal Renal Function Caused by Prolonged Environmental Exposure to Microcystin-LR
by Yuuka Hitsuda, Yoshihito Koto, Hideaki Kawahara, Koichi Kurata, Keisuke Yoshikiyo, Kohji Nishimura, Ayumi Hashiguchi, Hideaki Maseda, Kunihiro Okano, Norio Sugiura, Kazuya Shimizu and Hidehisa Shimizu
Toxics 2024, 12(8), 547; https://doi.org/10.3390/toxics12080547 - 27 Jul 2024
Viewed by 597
Abstract
Toxic algae in eutrophic lakes produce cyanotoxic microcystins. Prior research on the effect of microcystin-LR in the kidney utilized intraperitoneal injections, which did not reflect natural exposure. Oral microcystin-LR research has focused on renal function and histopathology without examining the molecular mechanisms. The [...] Read more.
Toxic algae in eutrophic lakes produce cyanotoxic microcystins. Prior research on the effect of microcystin-LR in the kidney utilized intraperitoneal injections, which did not reflect natural exposure. Oral microcystin-LR research has focused on renal function and histopathology without examining the molecular mechanisms. The present study aimed to evaluate the mechanism of microcystin-LR in the kidneys via oral administration in WKAH/HkmSlc rats over 7 weeks, alongside stimulation of the proximal tubular cells. Although there were no differences in the concentrations of plasma albumin, blood urea nitrogen, and creatinine, which are parameters of renal function, between the control and microcystin-LR-administrated rats, prorenin expression was significantly increased in the renal cortex of the rats administered microcystin-LR and the microcystin-LR-treated proximal tubular cells. The expression levels of (pro)renin receptor (PRR), transforming growth factor-β1 (TGFβ1), and α-smooth muscle actin (α-SMA) in the renal cortex did not differ significantly between the control and microcystin-LR-administered rats. However, the expression levels of prorenin were significantly positively correlated with those of PRR, TGFβ1, and α-SMA in the renal cortex of rats administered microcystin-LR. Additionally, a significant positive correlation was observed between the expression levels of TGFβ1 and α-SMA. Collectively, increased prorenin expression caused by the long-term consumption of microcystin-LR may initiate a process that influences renal fibrosis and abnormal renal function by regulating the expression levels of PRR, TGFβ1, and α-SMA. Full article
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